Should Every Cow Carry a Government Health Warning?

CHD is caused by atherosclerosis While the presence of underlying coronary artery-wall disease provides a necessary infrastructure for CHD, myocardial infarction and sudden death are rapid events. There is abundant evidence that the critical process in transmural myocardial infarction (Mitchell, 1978a) and in sudden death is thrombosis, often in association with plaque disruption (Davies & Thomas, 1984). Atherosclerosis is synonymous with lipid deposition When Virchow (1858) looked at clinically-relevant arterywall plaques he thought that they represented chronic inflammation. Observations showed him that all the

(H. L. Mencken) Whenever anyone says "it is generally agreed that ..." it invariably means that it is neither known or agreed. In any field where no progress appears to be occurring, it is always useful to look at the points on which there is indeed general agreement because they may well be wrong. Even a brief glance at medical history should give us a due sense of humility when we look at the "neat and plausible" solutions of the past that are now perceived to have been mere dogma. This should make us wonder which of our present beliefs will not only be discarded but be actively derided by the year 2000.
A cosy and plausible chain of beliefs about diet and coronary heart disease (CHD) has reached the "it is generally agreed" category and runs as follows: ?CHD is caused by atherosclerosis |l ?Atherosclerotic plaques are cholesterol deposits in artery walls ?Atherosclerosis can be produced in animals by lipid feeding ?A high serum cholesterol is a risk marker for CHD ?Dietary lipids determine serum cholesterol If one accepts that all these statements are true and that they belong to the same logic-chain, then two further statements arise: ?Dietary lipids cause coronary heart disease As we shall see, most of the statements set out here are either untrue or irrelevant.
CHD is caused by atherosclerosis While the presence of underlying coronary artery-wall disease provides a necessary infrastructure for CHD, myocardial infarction and sudden death are rapid events. There is abundant evidence that the critical process in transmural myocardial infarction (Mitchell, 1978a) and in sudden death is thrombosis, often in association with plaque disruption (Davies & Thomas, 1984).
Atherosclerosis is synonymous with lipid deposition When Virchow (1858) looked at clinically-relevant arterywall plaques he thought that they represented chronic inflammation. Observations showed him that all the layers of the artery wall were involved. The presence of 1 lymphocytes, plasma cells, giant cells, fibroblasts and calcium deposits would not have permitted him to lend his name to any description of atherosclerosis that regarded it merely as lipid deposition in the intima.
Atherosclerosis can be imitated in animals Vascular lesions produced by feeding fat reflect the erroneous concept of human disease which we have already discarded since they merely show intimal foam cell/ modified smooth-muscle-cell lesions which resemble clinically-irrelevant fatty streaks rather than multi-layer, multi-process, stenosing and thrombosing human lesions (Mitchell & Schwartz, 1965 Association does not imply causality, but cholesteroj has been assumed to play a prime causal role because o' the 'articles of faith' set out previously. Moreover, on^ can blame the victim's life-style and can set about tidying it up, whereas for other equally-powerful risk marked one has to blame his parents and his genes. For example' short stature and high blood pressure have both emerged from major studies (Logan et al. 1978;Mitchell* 1978b) as risk predictors and yet both of them oWe almost everything to inheritance and very little to environment. Social class is an extremely powerful mortality risk-marker (in the UK, the death-rates for men and women aged 15-64 years in the unskilled social class ^ are 2.5 times higher than in the professional social class I; Black et al. 1982). These are, however, not social classes but educational classes; in the USA, Hinkle et al (1966) found that asking healthy people about the duration and type of their education was just as powerful 3 predictor of CHD risk as cholesterol, smoking and hypertension. On these findings it would be as logical to assert that compulsory college education for all would halve the death toll from CHD as to make the more conventional claim that cholesterol-reduction would be similarly beneficial.
Serum cholesterol is determined by diet Cholesterol like urate, is an endogenous material which in a freerange society is genetically determined and is minimally related to diet (Neufeld & Goldbourt, 1983). It is true that dietary change will modify serum cholesterol and that between-population comparisons show that total fat intake and saturation-level of that fat are correlated with serum cholesterol (Keys, 1980), but if one makes withinpopulation comparisons, the influence of diet on cholesterol levels is minimal. Cholesterol is a marker of who you are rather than what you do.
The theoretical claim The case which is being put to the public rests on this series of statements, out of which emerges a rallying cry that poor diet causes coronary disease, so that by dietary manipulations we could prevent the epidemic of CHD. Before we examine the only way to test these claims, we need to be aware of information which is being used to lend support and credibility to them.
During the last 10 years, the USA coronary mortality has fallen by 25% (Harper, 1983) and there is an unseemly rush to claim the credit for this (prudent eating, better blood-pressure control, anti-smoking campaigns, coronary care units, jogging and weight reduction). The problem is that all sections of the USA community have been equally benefited and at the same time (old and young, rich and poor, black and white, men and women). I remain unconvinced that a poor black elderly woman living in Washington is likely to have changed her life style or been offered the advances in blood-pressure c?ntrol and coronary care to the same extent as a young, fluent white man from Scarsdale. Those who believe that they can 'explain' the decline in CHD in the USA by better health care would do well to ponder why, in a highly-developed, health conscious and disciplined ' country like Sweden, CHD incidence and mortality seem t? be increasing (Alfredsson & Ahlbom, 1983 who had a programme of advice aimed to reduce blood pressure, smoking and plasma lipids, to conquer obesity and to increase physical activity. The comparative group, who knew of course that they were "high risk" were simply sent back to their doctors for "usual care" (UC), but as in Finland, this 'control' group changed their behaviour markedly, so both groups showed a fall in plasma lipids. Table I shows the end-result, in that the "got-at" men did slightly worse in terms of overall mortality than the "laissez-faire" men.
WHO European Collaborative Group Study (1983) 49,781 men aged 40-59 working in 66 factories were recruited. The factories were paired and one of each pair was randomly allocated to receive special intervention.
Within an intervention factory the intention was to lower cholesterol by diet, to reduce smoking and weight, to increase physical activity and to control high blood pressure. Table II shows how the risk factors fared and Table III shows the effect on the pre-determined end-points. Special intervention is clearly not good news for Britons in that they fared worse in all these end-points than their fellows who were left alone. (Table IV) Non-dietary lipid trials The Lipid Research Clinics Coronary Primary Prevention Trial (1984) They screened 480,000 men and identified the 3806 with cholesterol levels in the top 5% of the distribution.
These men were all given cholesterol-lowering diets and only those whose serum lipids did not fall to predetermined levels went on into the oral cholestyramine versus placebo phase of the study. Thus the trial results are based on diet-resistant patients who were then followed for a mean of 7.4 years. The total deaths in the cholestyramine-treated group (n = 1906) were 68 and 71 in the placebo group (n = 1900), so screening half-amillion men and subjecting nearly 2,000 of them to 'treatment' for 7 years has 'saved' 3 lives. The trial organisers clearly perceived the unacceptability of a drug-based approach so wrote "the LRC-CPPT results and those of similar trials thus suggest that the risk of an initial CHD episode in hypercholesterolaemic middleaged men can be reduced by half with currently available appropriate cholesterol-lowering agents and diets" even though their trial offers no evidence on the value of diet.   What interests patients is staying alive and free from disability. They are not interested in risk-markers such as blood-lipids and blood pressure but only in their effect and in the benefit which modification of these factors will confer on them.
Once we have told our patients to stop smoking, then as scientists and men of commonsense, we have a duty to share our uncertainties about the other risk markers with them. If we do not do so, and they challenge us to produce evidence that by following the advice given by the Multiple Risk Factor Intervention Trial Research Group (1984) about diet, weight, activity and blood presslaborative Group, 1983 and the Lipid Research Clinic Group 1984) about diet, weight, activity and blood pressure control they will live longer or stay free from clinical CHD, then we cannot do so. The campaigners for mass prevention then turn on to another tack by saying: 'Even if it does no good it can do no harm'. I do not think that they have taken a broad enough view of what constitutes harm for there will be harm to our credibility as scientists and as health advisers. If we go public on diet and CHD on the basis of poor evidence we are weakening our position in respect of measures for which there is clear evidence: that everyone should be a non-smoker and that blood pressure control prevents strokes and heart failure. Over the centuries the public have been given so many crazy admonitions by "leaders" of medical opinion (on the evils of masturbation and of constipation; on the best way to treat mental illness, multiple sclerosis and breast cancer) that they cannot decide who to listen to and what they should do. If we fail in our duty to differentiate between what is known and what is merely believed, then the harm from such false advice is to our credibility, for as Mencken reminds us, "The most costly of all follies is to believe passionately in the palpably-nottrue"